Nitric oxide is responsible for oxidative skin injury and modulation of cell proliferation after 24h of UVB exposure.

MedLine Citation:

PMID:
22512358
Owner:
NLM
Status:
Publisher

Abstract/OtherAbstract:

Abstract Nitric oxide (NO) is produced by various mammalian cells and plays a variety of regulatory roles in normal physiology and in pathological processes. This article provides evidence regarding the participation of NO in UVB- induced skin lesions and in the modulation of skin cell proliferation following UVB skin irradiation. Hairless mice were subjected to UVB irradiation for 3 hs and the skin evaluated immediately, 6 and 24 hours postirradiation. The skin lipid peroxidation, and NO levels evaluated by chemiluminescence and iNOS and nitrotyrosine immunolabeling increased significantly 24h after irradiation and decreased under the treatment with aminoguanidine (AG). On the other hand, cell proliferation markers, PCNA and VEGF showed a strong labeling index when AG was used. The data indicate that NO mediates, at least in part, the lipid peroxidation and protein nitration and also promotes the down regulation of factors involved in cell proliferation. This work shows that the NO play an important role in the oxidative stress damage and on modulation of cell proliferation pathways in UVB irradiated skin.